Trypanosoma cruzi, the pathogen of Chagas disease, is an haemoflagellate belonging to the trypanosomatids, which are flagellates characterized by a kinetoplast (fig. 2.30, page 66). The pathogen is transmitted to man under natural conditions only by bloodsucking assassin bugs (Reduviidae: Heteroptera). Therefore, endemic Chagas disease is restricted to Middle and South America.

The vector bugs transmit the pathogen contaminatively via the faeces delivered immediately after engorgment (stercorarial trypanosomines). The metacyclic trypomastigotes enter the mammalian host via the stab wound or via the connective tissues of the mouth or the eyes when rubbed. The pathogen is unable to penetrate intact normal skin.

Development cycle of the pathogen (fig. 2.32, page 70): In the mammalian host, the invading trypomastigotes multiply inside macrophages as kryptomastigotes passing through four division cycles in about 4 days and then escape as circulating, briefly flagellated trypomastigotes. This form generalizes the infection and the pathogens now enter cells of various host tissues creating pseudocysts filled with kryptomastigotes. Circulating trypomastigotes establish the transferent phases of the disease.

Symptoms of the disease: A few days after an infective bite, a localized hypersensitivity reaction is often observed restricted to the original entrance site of the trypanosomes. This consists of oedema of the eyelid accompanied by a swelling of the regional maxillary lymphnodes and acute fever, a symptom trio called the Romaňa sign. The acute phase is followed by a symptomless latent phase, which may last several decades or even for the rest of the patients life. Otherwise, it is followed by the chronic phase during which pathogenic processes cause gradually deterioration of the tissues of the internal organs.

According to the symptomatic character of the disease (the nosodemes), the pathogens are classified as follows: myotropic strains lead to dystrophy of the heart muscle, neurotropic strains enter the visceral ganglia and cause enteromegalies, reticulotropic strains injure the liver, spleen or bone marrow. Thus, the course of the disease is markedly chronic. In addition to about 10% lethality in children, permanent serious injures appear mostly in middle-aged adults. As these adults are usually in the middle of their working lives, this lingering illness represents a serious social burden.

For diagnosis, among other measures, assassin bugs reared free of trypanosomes are allowed to feed on the patient. In positive cases, developing trypanosomes are seen in the faeces of the bug after a few days: xenodiagnosis. Lampit® and Rochagan® are available for chemotherapy. These drugs are taken orally but treatment is necessary daily for many months and has to be medically supervised because of possible side-effects. No suitable medicament is available for mass therapy. Immunological prophylaxis is still unavailable.

Development in the vector bug (fig. 2.32, page 70): the trypomastigotes are taken up with the blood, enter the anterior midgut or stomach and agglomerate there for a short time. An exchange of genes might occur at this stage, as evidenced by new combinations of isoenzymes. In the adjacent long midgut or intestine, the epimastigotes multiply and, having reached the rectal bladder, change again into metacyclic trypomastigotes, which are once more infective for the mammalian host. The uptake of blood activates the symbiotic bacteria located in the cells of the cardia at the entrance to the stomach and are mixed with the blood meal aiding its digestion. The symbionts reach the next generation contaminatively via the faeces.

The combined pattern of the various isoenzymes is called the zymodeme (fig. 2.35, page 75). It may aid the identification of certain trypanosome strains. The calculation of the similarity of principle zymodemes results in a dichotomically branched system or dendrogramme. Several dendrogrammes can be interpreted evolutionary as a kladogramme (fig. 2.47, page 90).

Assassin bugs are nocturnal and penetrate the hosts skin with their long piercing mouthparts: the mandibles with their strong barbs and the maxillae, which together form the wide food channel and a common small salivary channel. The maxillae bore into a blood capillary, which is reached by searching movements of up to 2.3 mm in depth. All larval stages feed on blood, requiring increasing amounts with time and at increased feeding depths. The winged imago is able to fly, but its mobility in search of food (feeding mobility) is limited. Predominantly, it breeds inside the abode of its victims, which, in case of human beings, is the inside of walls adjacent to bedding or in the thatching material on roofs.

Wild mammals, livestock and other domestic animals provide an almost unlimited potential natural reservoir for T. cruzi. However, predominantly only the opossum, dog and rats and mice are of epidemiological importance. Medical tranfusions of blood have led to the urbanisation of the disease. Conserved blood must be kept in mind as a possible source of infection. Silvatic and domestic transmission cycles occur, characterized by special pathogen-vector complexes (fig. 2.33, page 73).

Man is transferent only for a limited time with rare exceptions. However, the pathogen multiplies in assassin bugs and makes them permanently infective. Since all stages of the bugs feed on blood at least once during each instar, with infected bugs feeding more frequently, the loss of blood experienced by the host may be considerable in the long-term. In a nesting area, the bugs practise cannibalism and coprophagia. As a result, the infection rate in the bugs increases in the consecutive larval stages and frequently attains 30 % to 50 % in the imagines. Poor hygiene, encouraged by poverty, favours the spread of the infection and hinders its eradication.

The risk of infection is moderate in tolerable living conditions. The individual infection rate (IPC, infection rate per caput) has been calculated: 104 bites, infective or not, are necessary for one new infection. In the case of 20% infective bugs and 10 infective bites per night, 200 nights are needed for one new infection. The age at first infection is 6 months. Measures to lower the contact rate between man and assassin bugs are manditory prior to any control campaign.

The control of assassin bugs by insecticides requires great expenditure with regard to energy and cost and the effect is short-lived. Biological control by ichneumon flies (Telonomus spec. Hymenoptera: Scelionidae) or by entomopathogenic flagellates (Blastocrithidia spec.) and a yeast (Beauveria spec.) are under trial.